Figure 2.

Defective Gα_q protein but not the reduction in Gα_q level is responsible for the loss of a light response. (A) ERG recordings of Gα_q mutants. Flies trans-heterozygous for V303D and the deficiency Df(2R)Gαq1.3 displayed no light response. Mutants either homozygous for the Gα_q¹ mutation or trans-heterozygous for Gα_q¹ and V303D displayed a substantial response to light. (B) Western blot analyses of Gα_q protein level showed that Gα_q level is lower in Gα_q¹ mutants than in V303D homozygous mutants. TRP serves as a loading control. (C) The ERG recordings of V303D mutants expressing different Gα_q variants. Flies carrying homozygous V303D mutation, a GMR-Gal4 transgene, and different UAS-Gα_q transgenes were subject to ERG recording. Both the wild-type Gα_q and the mammalian mimic V303I transgenes rescued the ERG phenotype. For all ERG traces, event markers represent 5-sec orange light pulses, and scale bars are 5 mV. (D) Western blot measurement of Gα_q protein level in rescued lines. Gα_q level was restored to 40% of the wild-type level when GMR-Gal4 was used to drive Gα_q expression. INAD served as a loading control. Quantification of the Western blot results is given below. The complete genotypes are as follows: w¹¹¹⁸ (wt); w¹¹¹⁸; Gα_q^V303D (V303D); w¹¹¹⁸; Gα_q^V303D/Df(2R)Gαq1.3 (V303D/Df(2R)G); w¹¹¹⁸; Gα_q¹ (Gα_q¹); w¹¹¹⁸; Gα_q^V303D/Gα_q¹ (V303D/Gα_q¹); w¹¹¹⁸; Gα_q^V303D gmr-Gal4; UAS-Gα_q⁺; w¹¹¹⁸; Gα_q^V303D gmr-Gal4; UAS-Gα_q^V303D; w¹¹¹⁸; Gα_q^V303D gmr-Gal4; UAS-Gα_q^V303I.